Considerable evidence suggests that oxidative stress contributes to the etiology, pathogenesis, and aggressiveness of prostate cancer (PCa). Consequently dietary antioxidants, which inactivate reactive oxygen species and provide protection from oxidative damage, are considered important preventive agents against the development of PCa. However, the association between antioxidants and PCa has not been demonstrated consistently across epidemiological studies that took into account both dietary and supplement intake. The inconsistencies may result in part from failure to account for major sources of antioxidants in human diets that derive from many different chemical forms and confound this association. Dietary total antioxidant capacity (TAC) is a new concept that enables one to estimate the sum of protective properties of dietary antioxidants against oxidative stress. Whether or not dietary TAC estimates correctly reflect in vivo antioxidant status and oxidative stress depends on the completeness and validity of dietary intake data that include accurate food composition data. Our recent studies indicate that dietary TAC levels of Caucasian Americans (CA) are higher than those of African Americans (AA). According to the U.S. Cancer Statistics for 2003-2007, the incidence rates of PCa are 50% higher for AA than CA, while mortality rates are 150% higher for AA. Factors proposed to explain this disparity include racial differences in PCa screening, access to care or care seeking behaviors, and etiologic and pathogenetic factors that influence PCa biology and aggressiveness. The racial disparity in PCa aggressiveness may be in part attributed to racial differences in antioxidant intake. However, limited information is available on the nutritional modulation of PCa aggressiveness. Thus, the objective of the proposed study is to determine the extent to which dietary TAC predicts PCa aggressiveness. The central hypothesis is that validation of a novel TAC tool will enable prediction of the risks of PCa mediated by oxidative stress. Our working hypothesis is that racial differences in PCa aggressiveness are in part the result of racial differences in antioxidant intake. To test the overall hypothesis, our specific aims are to: 1) determine the impact of dietary TAC on aggressiveness of newly diagnosed PCa; 2) determine whether dietary TAC level of PCa patients is associated with antioxidant-redox status in plasma, urinary, and PCa tissue samples; and 3) evaluate major dietary, sociodemographic, and lifestyle factors contributing to racial differences in dietary TAC of PCa patients by utilizing data on newl diagnosed PCa patients recruited through North Carolina-Louisiana Prostate Cancer Project. This project will provide important information on dietary TAC as a modifiable lifestyle factor among men diagnosed with PCa, and the extent to which it differs by race. Identification of dietary effects on PCa aggressiveness would suggest the importance of lifestyle behavioral factors in PCa outcome. Furthermore, the determination of racial differences in dietary behaviors may provide information that could be used to develop appropriate interventions to lower the risk of fatal PCa and reduce racial disparities in PCa mortality.